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Kajitani, Koji,Ken-Ichi, Honda,Terada, Hiroyuki,Yasui, Tomoyo,Sumi, Toshiyuki,Koyama, Masayasu,Ishiko, Osamu Asian Pacific Journal of Cancer Prevention 2015 Asian Pacific journal of cancer prevention Vol.16 No.18
The p53 gene is inactivated by the human papillomavirus (HPV) E6 protein in the majority of cervical cancers. Treatment of HeLa S3 cells with siRNA for HPV E6 permitted adenovirus-mediated transduction of a p53 gene linked to an upstream estrogen response element (ERE). Our previous study in non-siRNA treated HHUA cells, which are derived from an endometrial cancer and express estrogen receptor ${\beta}$, showed enhancing effects of an upstream ERE on adenovirus-mediated p53 gene transduction. In HeLa S3 cells treated with siRNA for HPV E6, adenovirus-mediated transduction was enhanced by an upstream ERE linked to a p53 gene carrying a proline variant at codon 72, but not for a p53 gene with arginine variant at codon 72. Expression levels of p53 mRNA and Coxsackie/adenovirus receptor (CAR) mRNA after adenovirus-mediated transfer of an ERE-linked p53 gene (proline variant at codon 72) were higher compared with those after non-ERE-linked p53 gene transfer in siRNA-treated HeLa S3 cells. Western blot analysis showed lower ${\beta}$-tubulin levels and comparatively higher p53/${\beta}$-tubulin or CAR/${\beta}$-tubulin ratios in siRNA-treated HeLa S3 cells after adenovirus-mediated ERE-linked p53 gene (proline variant at codon 72) transfer compared with those in non-siRNA-treated cells. Apoptosis, as measured by annexin V binding, was higher after adenovirus-mediated ERE-linked p53 gene (proline variant at codon 72) transfer compared with that after non-ERE-linked p53 gene transfer in siRNA-treated cells.
Eiji Kondo,Tsutomu Tabata,Nao Suzuki,Daisuke Aoki,Hideaki Yahata,Yoshio Kotera,Osamu Tokuyama,Keiichi Fujiwara,Eizo Kimura,Fumitoshi Terauchi,Toshiyuki Sumi,Aikou Okamoto,Nobuo Yaegashi,Takayuki Enomo 대한부인종양학회 2020 Journal of Gynecologic Oncology Vol.31 No.6
Objective: In this study we sought to investigate the clinical factors that affect post progression survival (PPS) in patients with recurrent or persistent clear cell carcinoma (CCC). We utilized the JGOG3017/Gynecological Cancer InterGroup data to compare paclitaxel pluscarboplatin (TC) and irinotecan plus cisplatin (CPT-P) in the treatment of stages I to IV CCC. Methods: We enrolled 166 patients with recurrent or persistent CCC and assessed the impactof variables, including platinum sensitivity, treatment arm, crossover chemotherapy, primarystage, residual tumor at primary surgery, performance status, ethnicity, and tumor reductionsurgery at recurrence on the median of PPS in patients with recurrent or persistent CCC. Results: A total of 77 patients received TC, and 89 patients received CPT-P. The median PPSfor patients with platinum-resistant disease was 10.9 months, compared with 18.8 monthsfor patients with platinum-sensitive disease (hazard ratio [HR]=1.88; 95% confidence interval[CI]=1.30–2.72; log-rank p<0.001). In the multivariate analysis, the platinum sensitivity(resistant vs. sensitivity; HR=1.60; p=0.027) and primary stage (p=0.009) were identified asindependent predictors of prognosis factors for PPS in recurrent or persistent CCC. Conclusions: Our findings revealed that platinum sensitivity and primary stage are clinicalfactors that significantly affect PPS in patients with recurrent or persistent CCC as well as other histologic subtypes of ovarian cancer. PPS in patients with recurrent CCC shouldestablish the basis for future clinical trials in this population.